The monocyte product, interleukin-1 (IL-1), provides a critical immunomodulatory signal during the immune response to infection. The investigator's laboratory effort is devoted to understanding the regulation of IL-1 synthesis. They have established a tumor model system for studying expression of IL-1 in a homogeneous, clonal cell population. Previous results of the laboratory have utilized this system to show that expression of IL-1 activity is an inducible function, that during monocyte activation, there is an accumulation of IL-1-beta mRNA, and that glucocorticoids block the accumulation of IL-1-beta mRNA. Their previous results suggest that IL-1 transcription changes during monocyte activation, and that glucocorticoids modulate transcription of the IL-1 genes. They now propose to extend these studies to the IL-1 gene. More importantly, they propose to establish that IL-1 gene are regulated at the level of transcription and determine whether IL-1 gene activation is accompanied by changes in DNase I sensitivity. In separate studies, they have discovered that translation of IL-1 protein is regulated. Although compounds that increase cellular cAMP do not influence accumulation of IL-1 mRNA, they effectively inhibit IL-1 protein synthesis. They propose to investigate the nature of the translational regulation of IL-1 synthesis, by examining the translational apparatus of cells with elevated cAMP, by analyzing the possible translational control sequences within IL-1 mRNA, and by searching for possible alterations in splicing of IL-1 mRNA. Several laboratories have reported that monocytes can be infected with retroviruses. The investigator has discovered that monocytes can be infected by culturing cells with hepatitis B virus (HBV)-containing serum and that IL-1 expression by HBV-exposed monocytes is blocked. The suppressive effect of HBV-containing serum is mediated by virion that was found to replicate in the HBV-exposed monocyte. They have propose to determine the specificity of the virus-mediated changes in the immune functions of HBV-infected monocyte, and to determine the mechanism whereby the virion inhibits IL-1 expression.